I remember Judy Mikovits was speaking about finding the proper reservoir of the virus. Perhaps I am naive from the point of virology and biology but I remember well that only the first 4 years I felt pathological symptoms outside of my neuraxis. The last 8 years all my symptoms are so to speak "located" in the brain. Perhaps the WPI study tested "fresh" patients and this one the patients with XMRV for long time well hidden against the immune system in brain tissue. I know everyone with ME/CFS has individual experience with his own symptoms and his own perspective but I would prefer if some study found something pathological in the tissue from brain biopsy or in cerebrospinal fluid.

Why is age of blood an issue? WPI found XMRV in 25 year old samples. Yes WPI re-ran their samples many times (which they did not report initially), but by your reasoning they should not have had positives (unless it was some type of HERV reaction they actually found in those old samples?). Anyway, if WPI did get XMRV positives from old blood, they should have had some hits even on the first run, and so Kerr should have gotten some positives in this study. Also, this study was able to get hits on a known positive as well as carefully spiked positives. That says their test worked at least to some degree.

Also, they required 16 antigen copies? Didn't the IC study work with 1 single copy? Interesting, this was a less sensitive PCR test than the IC study.

The serology (antibody) testing is for MuLV and not specific to XMRV. Even activated HERVs can produce a positive. Using serology and saying that proves something is a bit of a dodge. So now people are believing serology tests are specific for XMRV, but that is wrong. Serology is supportive only and not conclusive.

What virus indeed. My guess is that WPI has found a novel MuLV type retrovirus or a HERV, and not XMRV at all, so as replication/validation testing gets more and more specific for XMRV they will have less and less success. That is probably why only serology testing is working. Or possibly serology is picking up a HERV expressed in CFS (which also could include RT). Some smart lab who sequences the antigen will figure this out. Also, note that neither Kerr nor WPI used the pol gene, why are they avoiding the stable portion of the genome?

Who are you waiting for? This is science, there are no 'powers to be', certainly not WPI, they are disqualified scientifically from confirming their own finding, and are biased in any response to outside efforts. These collaborating labs ARE the powers you are waiting for, and this IS the evidence for or against XMRV that we are waiting for. The score right now is not looking good for XMRV in CFS.

There is still good research going on right now in the CFS community and some promising leads for other explanations. XMRV is not the only game in town.

Their interest in replicating has nothing to do with what they will find. If XMRV was a false finding, the Belgian study will likely also not find any XMRV in CFS. The final outcome is still unknown by ANYONE, we just have to wait.

I will take a cup of Chamomile, read a good book, and continue trying to be objective and not to get too emotionally involved in this process, it takes years sometimes.

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hi Kurt The age of the blood is relevant because if extreme care is not taken at the point of sample collection cell lysis osmolarity changes etc release DNase which degrade the DNA so the older the blood the more degredation takes place.The older anticagulants inhibited tag polymerase and played havok with PCR so if the blood is say 15 years old the older anticoagulants were likely to be used.Now we know what happens when blood is collected in outpatients or in pathology cell lysis is very commonplace. The longer the blood is initially kept at ambient temperature the more chance of degredation processes starting.Rate of thawing also effects degredation-cryolysis.Dna in sera has even more problems due to deamination and hydrolytic cleavage.The age of blood also affects differnt types of RNA differently including viral RNA .These patients were in the NHS if the blood was taken by doctors probably juniors the situation could be even worse.

originally posted by Kurt;"What virus indeed. My guess is that WPI has found a novel MuLV type retrovirus or a HERV, and not XMRV at all, so as replication/validation testing gets more and more specific for XMRV they will have less and less success. That is probably why only serology testing is working. Or possibly serology is picking up a HERV expressed in CFS (which also could include RT). Some smart lab who sequences the antigen will figure this out. Also, note that neither Kerr nor WPI used the pol gene, why are they avoiding the stable portion of the genome?"

So Kurt, if this hypothesis is correct, then WPI would have found something in 98% of PWC and 4% of healthy controls. Am I understanding that correctly.

That would be fine with me. It would still be a significant finding, poiniting (probably) to a causal factor, or at least a biomarker. So the task over the next while will be to identify what that something is. If it's not XMRV who cares. A biomarker is a biomarker.

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Yes, they probably found something. And those high numbers are not unique, remember the ciguatera epitope? That was found in 96% of PWC. But if the XMRV validation studies continue to be negative, then likely they found something besides XMRV.

An HERV that can infect other cells?
WPI sequenced virus from patient samples differed by six nucleotides from an XMRV strain found in prostate cancer. This is less than the difference between two different XMRV prostate cancer strains. How is that a completely different virus let alone an HERV?
You say the score is not looking good based on studies that can't find XMRV in ONE SINGLE SAMPLE and use spiked controls rather than an actual patient control?

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I recently addressed this in the Cooperative test thread, and yes while most HERVs lack the pol gene required to replicate externally, it is conceivable that a HERV could be amplified through DNA activation if a culture study happens to use a cell line known to produce the target antigen, and a triggering protein as part of the amplification. And WPI used a prostate cancer cell line which is interesting. I don't know if their amplification included a triggering protein, so am not saying that happened, just that it is a possible alternate explanation that has to be evaluated experimentally.

They had a real control from Silverman, but using spiked controls is a normal procedure. I would imagine at some point WPI did that as well, in fact a known positive control should probably be run with every batch.

What really bothers me is it's published in Retrovirology for the whole world to see. How do these studies then get discredited should there be grounds to?

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When a research line gets discredited usually the journals publishing the discredited studies will publish a retraction. But we are quite far off from that, there is not a sufficient body of studies yet.

hi Kurt The age of the blood is relevant because if extreme care is not taken at the point of sample collection cell lysis osmolarity changes etc release DNase which degrade the DNA so the older the blood the more degredation takes place.The older anticagulants inhibited tag polymerase and played havok with PCR so if the blood is say 15 years old the older anticoagulants were likely to be used.Now we know what happens when blood is collected in outpatients or in pathology cell lysis is very commonplace. The longer the blood is initially kept at ambient temperature the more chance of degredation processes starting.Rate of thawing also effects degredation-cryolysis.Dna in sera has even more problems due to deamination and hydrolytic cleavage.The age of blood also affects differnt types of RNA differently including viral RNA .These patients were in the NHS if the blood was taken by doctors probably juniors the situation could be even worse.

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OK, so the original collection procedure might have been better in the 25 year-old blood taken by Peterson's office than the 15 year old UK blood? Yes, that certainly is an alternate explanation. Yet another variable that needs to be run down.

Yes, they probably found something. And those high numbers are not unique, remember the ciguatera epitope? That was found in 96% of PWC. But if the XMRV validation studies continue to be negative, then likely they found something besides XMRV.

I recently addressed this in the Cooperative test thread, and yes while most HERVs lack the pol gene required to replicate externally, it is conceivable that a HERV could be amplified through DNA activation if a culture study happens to use a cell line known to produce the target antigen, and a triggering protein as part of the amplification. And WPI used a prostate cancer cell line which is interesting. I don't know if their amplification included a triggering protein, so am not saying that happened, just that it is a possible alternate explanation that has to be evaluated experimentally.

They had a real control from Silverman, but using spiked controls is a normal procedure. I would imagine at some point WPI did that as well, in fact a known positive control should probably be run with every batch.

When a research line gets discredited usually the journals publishing the discredited studies will publish a retraction. But we are quite far off from that, there is not a sufficient body of studies yet.

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The last herv shown to be infective was about the time we diverged from chimps whatever the WPI found was infective and other workers have found exactly the same virus with the same base sequence. Even the opponents of xmrv as causative agent accept its existence.Everyone seems to forget that the WPI used a different patient cohort most british patients when diagnosed have idiopathic chronic fatigue.Feduka cant differentiate these from CFS and these guys pretend its feduka when in reality its oxford.you also cant get viruses from cells in 18 hours when it takes those cells two weeks to produce such virus When you say there are no powers that be in science I am afraid that you are being niave.You dont use a control group with ilnesses know to be related to endogenous gammas if you are seriously trying to find a very closely related endogenous one

The U.S. Department of Health and Human Services Blood XMRV Scientific Research Working Group has been established to delineate the research studies that should be undertaken to evaluate whether XMRV represents a risk to the safety of the blood supply. As a first step in this evaluation, analytical panels are being developed by the National Heart, Lung, and Blood Institute Retrovirus Epidemiology Donor Study-II (REDS-II) that will allow for multiple laboratories to standardize methods to optimize sensitive detection of XMRV proviral DNA and viral RNA. Once methods are standardized, these same laboratories plan to test coded panels of blood samples obtained primarily from healthy blood donors and from CFS patients who have been reported to be positive for XMRV.

We look forward to the results of this study and urge that it be completed expeditiously, especially in light of this report from the U.K. In the meantime, be prepared to read about more studies with conflicting findings. Rather than simply accept or dismiss new information, we will help make sense of why discrepant results occur.

The last herv shown to be infective was about the time we diverged from chimps whatever the WPI found was infective and other workers have found exactly the same virus with the same base sequence. Even the opponents of xmrv as causative agent accept its existence.Everyone seems to forget that the WPI used a different patient cohort most british patients when diagnosed have idiopathic chronic fatigue.Feduka cant differentiate these from CFS and these guys pretend its feduka when in reality its oxford.you also cant get viruses from cells in 18 hours when it takes those cells two weeks to produce such virus When you say there are no powers that be in science I am afraid that you are being niave.You dont use a control group with ilnesses know to be related to endogenous gammas if you are seriously trying to find a very closely related endogenous one

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I did not say infective, rather that there are ways to activate a HERV with an amplification culture. A culture process might activate a HERV rather than culture an exogenous virus. But I am not doubting that XMRV exists, just trying to illustrate the types of issues that have to be addressed to reach a credible scientific consensus on the WPI study.

True about patient criteria, but with that large of a sample they should have had many true CFS patients.

Good point about 18 hours for amplification, how long did WPI amplify? I am assuming that was documented or stated somewhere, and that the Kerr study tried to replicate that. So that is the point. Also, how long does HERV activation take?

Many competing labs have to weigh in on this, including some independent labs with no agendas. That is what I means by powers that be, there is no final arbitrator here, no authority figure. Maybe things look different in the UK, but here in the US things are usually a bit of a free-for-all.

I agree about Kerr's control group, that made little sense except that it was probably a convenient sample available to them.

ukxmrv- yeah, that's what I mean. Nothing in this new study should be construed as a "replication study." This kind of thing will go on for a while, with various researchers using their own proprietary or favored method of PCR (different primers, different proteins, etc.) and finding different results, claiming that their test therefore proves it doesn't exist in CFS/ME. The headlines piss me off because most people don't go further than the headlines and look at the science, but that's "news" for you.

I don't think some kind of disclaimer would go amiss at the top of the first post. It is, after all, just a post and not any kind of official release of that study or the press release. The release uses such definitive language which seems to speak for the ME community that I'm sure most people would read no further.

Could we direct people to view the later conversation off the top?

Something like this:

* SOME VERY SERIOUS CONCERNS ABOUT THE VALIDITY OF THIS STUDY HAVE BEEN RAISED ~ THAT DISCUSSION BEGINS ON PAGE 6 *

or whatever page it does begin on. (Don't want to navigate away from this page and lose my post.)

Thanks again, Orla, for bringing this to our attention so that we could give it the necessary critique.

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Hi Koan,

Good point. These monster threads are hard to concentrate on for many of us.

Please note that the forum software allows you to say how many posts show per page. So my page numbers do not match up with yours.

Using article numbers is more bulletproof (though maybe not if you merge threads).

%&^&%&! I was just starting to feel really good about all of this. No ulterior motives with Kerr and Gow. Kerr was very careful with his gene expression work - he crossed and dotted every T. Kerr is working closely with the WPI - he won that grant with them and he's doing that other study (apparently). I can't imagine he would lend his name to bad study. Ironically Gow was the other researcher that couldn't find De Freitas virus 25 years ago.

Stil,l the most salient point of the Science Paper was the ability of the WPI researchers to put a clean cell next to a cell packed full of that XMRV (or whatever it is) and then watch that clean cell get infected and they were able to snap a picture of a virus budding out of that previously clean cell. If it wasn't XMRV it must have been something else - but something appeared to be growing in there. Until someone can explain to me that thats not the crux - or explain it away - I'm going to keep focused on that.

If its an muLv virus fine. If its an endoretrovirus that's escaped and is infecting cells - that's probably fine too because I don't they've found one that can do that yet.

It's not all bad news! (Actually I think there may even be some really good news buried deeply in these results)....

Like everyone else, I was disappointed when I heard the news of this study, but I'd been bracing myself for bad news... I was expecting more bad news along the way, and I'd already privately started thinking that XMRV might not be the answer we've all been hoping for... especially as the private blood tests are coming back at 'only' 50% positive.

But, actually, this latest study has given me more encouragement than I had before it, not less!

For a quick over-view of where we are right now:
First of all, we know that about 50% of UK patients are getting tested positively when getting their blood tested privately. This is about the same figure as the USA results. (This is based on anecdotal reports from the patients themselves).
So, even if the 'experts' can't find it, we know that this virus exists in the UK, no matter what the Wessely study found.

Once the knowledge of this virus is out, as it is now, the genie can't be put back in the bottle. This virus is on our side now... we have real tangible proof of a new virus, which can't be disputed, even by Wessely. And it's now being investigated as a huge new phenomena, with huge amounts of funds going into it in the USA.

The first UK study, The Imperial College study by Wessely & co, showed no sign of any XMRV virus in any of the healthy 'normal' UK population... zilch, nada, nothing, zero... And we are all confident to ignore that study because we know it was flawed.
The second study, by Kerr & co, has found antibodies in the 'normal' controls, but not the ME patient blood (trust us in the UK to get it the wrong way round!)

This latest finding has two major implications which is why I am encouraged by it:
1. XMRV HAS BEEN DISCOVERED IN THE UK... They have now found the virus in the UK! Or at least antibodies to it! (I don't know why more of a fuss hasn't been made of this by the research team of by us lot!) I mean, this is really big news! XMRV is in the UK - why isn't this on the front page of all the newspapers in the morning, like the flawed Wessely study was! And another important point is that the percentage of the normal controls which tested positive for antibodies is exactly 4% - exactly the same as the WPI study - which is extraordinary, and i think significant! (26 out of 565 = 4.6%)
2. The fact that no virus was found in the ME patient blood also seems to be significant to me. Significant because it suggests that the study was flawed. (We'd expect at least 4% positive testing - the same as the control group) There may have been many reasons why the ME patient blood may have been made useless e.g. storage, handling etc (Also, and I can't help feeling paranoid that the world is against me here, but if the ME patients are all from a certain type of clinic, then maybe all the Canadian definition ME patients - i.e. post exertional malaise - had dropped out of the clinics because they were using GET techniques which were making them more ill - so maybe the only patients left in the clinics did not experience any post exertional malaise - but this wouldn't explain the discrepancy with the normal population results)

At least this team acknowledged that they had strange results and acknowledged that they need to more closely work with the WPI and standardize their tests.

So this all seems like good news to me!
So lets not be disheartened yet!

One other things is that the WPI is creating better tests for the public testing, and is going to re-test all their past tests with the better quality test.
This might mean that 60% or 70% of private blood testing ends up testing positive for XMRV (I'm being optimistic hear for the sake of discussion), in which case ME being associated with XMRV becomes a no brainer!

Please could anyone pick up on any points that I may have got incorrect. (Much appreciated.)

A new retrovirus, xenotropic murine leukaemia virus-related virus (XMRV), first identified in tumor tissue of individuals with prostate cancer, was subsequently found in 68 of 101 US patients with chronic fatigue syndrome (CFS). XMRV was not detected in blood samples of 186 confirmed CFS patients in the United Kingdom. A second independent study in the UK (pdf) has also failed to reveal XMRV in CFS patients.

The subjects of this study were confirmed CFS patients from St George’s University of London, Barts and the London Hospital Trust, and Glasgow Caledonian University. A total of 170 serum samples from CFS patients and 395 controls were used. A polymerase chain reaction assay was devised that could detect as little as 16 copies of proviral XMRV DNA (viral DNA integrated into human chromosomal DNA). No XMRV sequences were detected in 142 CFS samples and 157 controls.

A second method was then used to search for evidence of XMRV: the patient serum samples were examined for the presence of antibodies that could block infection of cells with the virus. Cells were infected with XMRV in the presence of serum from CFS patients or control patients. Included were sera known to block XMRV infection to ensure that the assay functioned normally. None of 142 CFS samples contained antibodies that could block XMRV infection of cells. In contrast, 22 samples out of 157 controls (14%) were identified that contained neutralizing activity. One of 28 CFS serum samples from a separate cohort was found to contain XMRV neutralizing activity; none of the 12 control sera could block XMRV infection.

These results could be interpreted to mean that XMRV infection occurs in the general population, confirming the observations of the first US study. However, the sera from the second UK study also blocked the infectivity of viruses other than XMRV, including those containing envelope proteins from vesicular stomatitis virus. The authors believe that the neutralizing activity in the control sera is not specific for XMRV. These antibodies were probably induced by infection with another virus.

The results obtained with these samples do not provide evidence for an association of XMRV infection and CFS. This does not eliminate a role for XMRV in CFS. As the authors write:

The publication of these results has promoted much discussion and controversy amongst CFS researchers and patients alike, and has highlighted the need for additional investigations in this area. Following the findings reported here, it would seem a prudent next step for subsequent studies to compare samples and protocols between different laboratories around the world.

It’s time to put aside arguments over the competence of laboratories to carry out polymerase chain reaction and work towards understanding the role of XMRV in human disease. The three laboratories who have published their findings on XMRV in humans should exchange their samples to confirm the findings. Compelling answers will only come from far more extensive global studies of the prevalence of XMRV in CFS and control populations are clearly needed.

%&^&%&! I was just starting to feel really good about all of this. No ulterior motives with Kerr and Gow. Kerr was very careful with his gene expression work - he crossed and dotted every T. Kerr is working closely with the WPI - he won that grant with them and he's doing that other study (apparently). I can't imagine he would lend his name to bad study. Ironically Gow was the other researcher that couldn't find De Freitas virus 25 years ago.

Stil,l the most salient point of the Science Paper was the ability of the WPI researchers to put a clean cell next to a cell packed full of that XMRV (or whatever it is) and then watch that clean cell get infected and they were able to snap a picture of a virus budding out of that previously clean cell. If it wasn't XMRV it must have been something else - but something appeared to be growing in there. Until someone can explain to me that thats not the crux - or explain it away - I'm going to keep focused on that.

If its an muLv virus fine. If its an endoretrovirus that's escaped and is infecting cells - that's probably fine too because I don't they've found one that can do that yet.

It's not all bad news! (Actually I think there's some really good news buried deeply in these results)....

Like everyone else, I was disappointed when I heard the news of this study, but I'd been bracing myself for bad news... I was expecting more bad news along the way, and I'd already privately started thinking that XMRV might not be the answer we've all been hoping for... especially as the private blood tests are coming back at 'only' 50% positive.

But, actually, this latest study has given me more encouragement than I had before it, not less!

For a quick over-view of where we are right now:
First of all, we know that about 50% of UK patients are getting tested positively when getting their blood tested privately. This is about the same figure as the USA results. (This is based on anecdotal reports from the patients themselves).
So, even if the 'experts' can't find it, we know that this virus exists in the UK, no matter what the Wessely study found.

Once the knowledge of this virus is out, as it is now, the genie can't be put back in the bottle. This virus is on our side now... we have real tangible proof of a new virus, which can't be disputed, even by Wessely. And it's now being investigated as a huge new phenomena, with huge amounts of funds going into it in the USA.

The first UK study, The Imperial College study by Wessely & co, showed no sign of any XMRV virus in any of the healthy 'normal' UK population... zilch, nada, nothing, zero... And we are all confident to ignore that study because we know it was flawed.
The second study, by Kerr & co, has found antibodies in the 'normal' controls, but not the ME patient blood (trust us in the UK to get it the wrong way round!)

This latest finding has two major implications which is why I am encouraged by it:
1. XMRV HAS BEEN DISCOVERED IN THE UK... They have now found the virus in the UK! Or at least antibodies to it! (I don't know why more of a fuss hasn't been made of this by the research team of by us lot!) I mean, this is really big news! XMRV is in the UK - why isn't this on the front page of all the newspapers in the morning, like the flawed Wessely study was! And another important point is that the percentage of the normal controls which tested positive for antibodies is exactly 4% - exactly the same as the WPI study - which is extraordinary, and i think significant! (26 out of 565 = 4.6%)
2. The fact that no virus was found in the ME patient blood also seems to be significant to me. Significant because it suggests that the study was flawed. (We'd expect at least 4% positive testing - the same as the control group) There may have been many reasons why the ME patient blood may have been made useless e.g. storage, handling etc (Also, and I can't help feeling paranoid that the world is against me here, but if the ME patients are all from a certain type of clinic, then maybe all the Canadian definition ME patients - i.e. post exertional malaise - had dropped out of the clinics because they were using GET techniques which were making them more ill - so maybe the only patients left in the clinics did not experience any post exertional malaise - but this wouldn't explain the discrepancy with the normal population results)

At least this team acknowledged that they had strange results and acknowledged that they need to more closely work with the WPI and standardize their tests.

So this all seems like good news to me!
So lets not be disheartened yet!

One other things is that the WPI is creating better tests for the public testing, and is going to re-test all their past tests with the better quality test.
This might mean that 60% or 70% of private blood testing ends up testing positive for XMRV (I'm being optimistic hear for the sake of discussion), in which case ME being associated with XMRV becomes a no brainer!

Please could anyone pick up on any points that I may have got incorrect. (Much appreciated.)

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Bob, thank you very much for your perspective. It is great that you could find some positive side to the study and I dig the fact that 4% of the control had some + XMRV material. Indeed it is a good sign. Why did the supposedly ME population didn't test +? Would it be wrong cohort- let's call it Wessley cohort, depressed patients and truly misdiagnosed patients, or perhaps patients that may have ME but their viral load is so low that it is not detectable.
Could it be that the methodology was mishandled, for instance, primers, frozen samples, or samples that sat on the countertop for too long? (I am no scientist here so looking forward to hear Dr Vernon, Klimas and Mikovits' opinions.

It's not all bad news! (Actually I think there may even be some really good news buried deeply in these results)....

Like everyone else, I was disappointed when I heard the news of this study, but I'd been bracing myself for bad news... I was expecting more bad news along the way, and I'd already privately started thinking that XMRV might not be the answer we've all been hoping for... especially as the private blood tests are coming back at 'only' 50% positive.

But, actually, this latest study has given me more encouragement than I had before it, not less!

For a quick over-view of where we are right now:
First of all, we know that about 50% of UK patients are getting tested positively when getting their blood tested privately. This is about the same figure as the USA results. (This is based on anecdotal reports from the patients themselves).
So, even if the 'experts' can't find it, we know that this virus exists in the UK, no matter what the Wessely study found.

Once the knowledge of this virus is out, as it is now, the genie can't be put back in the bottle. This virus is on our side now... we have real tangible proof of a new virus, which can't be disputed, even by Wessely. And it's now being investigated as a huge new phenomena, with huge amounts of funds going into it in the USA.

The first UK study, The Imperial College study by Wessely & co, showed no sign of any XMRV virus in any of the healthy 'normal' UK population... zilch, nada, nothing, zero... And we are all confident to ignore that study because we know it was flawed.
The second study, by Kerr & co, has found antibodies in the 'normal' controls, but not the ME patient blood (trust us in the UK to get it the wrong way round!)

This latest finding has two major implications which is why I am encouraged by it:
1. XMRV HAS BEEN DISCOVERED IN THE UK... They have now found the virus in the UK! Or at least antibodies to it! (I don't know why more of a fuss hasn't been made of this by the research team of by us lot!) I mean, this is really big news! XMRV is in the UK - why isn't this on the front page of all the newspapers in the morning, like the flawed Wessely study was! And another important point is that the percentage of the normal controls which tested positive for antibodies is exactly 4% - exactly the same as the WPI study - which is extraordinary, and i think significant! (26 out of 565 = 4.6%)
2. The fact that no virus was found in the ME patient blood also seems to be significant to me. Significant because it suggests that the study was flawed. (We'd expect at least 4% positive testing - the same as the control group) There may have been many reasons why the ME patient blood may have been made useless e.g. storage, handling etc (Also, and I can't help feeling paranoid that the world is against me here, but if the ME patients are all from a certain type of clinic, then maybe all the Canadian definition ME patients - i.e. post exertional malaise - had dropped out of the clinics because they were using GET techniques which were making them more ill - so maybe the only patients left in the clinics did not experience any post exertional malaise - but this wouldn't explain the discrepancy with the normal population results)

At least this team acknowledged that they had strange results and acknowledged that they need to more closely work with the WPI and standardize their tests.

So this all seems like good news to me!
So lets not be disheartened yet!

One other things is that the WPI is creating better tests for the public testing, and is going to re-test all their past tests with the better quality test.
This might mean that 60% or 70% of private blood testing ends up testing positive for XMRV (I'm being optimistic hear for the sake of discussion), in which case ME being associated with XMRV becomes a no brainer!

Please could anyone pick up on any points that I may have got incorrect. (Much appreciated.)

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So many good points here Bob. Straight to the point and explained in simple terms. Thank God someone here did explain it simply for the non scientists amongst us. One thing about no positives being found in the "CFS" group but 4% in the healthy controls is it makes me more suspicious about the cohorts and also makes me wonder whether the blood samples were pre screened before this study or indeed at any time in the past. It makes no sense that you wouldn't find 4% positive in the "CFS" patients but would find 4% in the healthy population. However there seemed to be a few different places providing the blood samples. This could explain the variance of results. They are reporting an overall result from a selection of different sample providers - is that true? Or did Kerr supply all the samples - I don't think that's how I read it.

Anyway it is obvious that the main aim of this study is headlining. How they came to their conclusions will not affect the press reporting the "result". I really feel that some reputable people have been duped here and now have their names on this study in an attempt to poke a sword into the backs of the ME community.

Like you say, at least it is confirmed to be present within these shores. I do worry about the June Kerr study going ahead though. It looks as though the plan is to rush out a load of flawed studies then pull the plug on any further ones going ahead. Hope the WPI/ Kerr study is a done deal.

There were a lot of onside ME people in this study including Abhijit Chaudri and Kerr, I just cant understand how or why they got duped into this. Anyone got any suggestions.

The thing about the WPI study is that didn't they have samples that tested positive not only at WPI but also at the Cleveland Clinic AND NIC? So that means three separate labs validated the WPI findings. I think we can be certain XMRV or something exists. It's another question as to whether it's in a different form in the UK.......I hope that WPI will put out a press release tomorrow and perhaps we'll learn more then. ~Fern

That's true the Cleveland Clinic looked at a small # of samples - and they came up positive. These studies were much bigger but what a puzzle it is. The WPI is clearly doing a different test than these studies.

I changed the title of the thread because I found it makes a big difference to search engine results - altho these results are nothing to be happy about. Dr. Vernon's response will be most instructive.